Maternal Physiological Adaptations Research Articles

Pregnancy-related maternal physiological adaptations and fetal chemical exposure

Prenatal life represents a susceptible window of development during which chemical exposures can permanently alter fetal development, leading to an increased likelihood of disease later in life. Therefore, it is essential to assess exposure in the fetus. However, direct assessment in human fetuses is challenging, so most research measures maternal exposure. Pregnancy induces a range of significant physiological changes in women that may affect chemical metabolism and responses. Moreover, placental function, fetal sex, and pregnancy complications may further modify these exposures. The purpose of this narrative review is to give an overview of major pregnancy-related physiological changes, including placental function and impacts of pregnancy complications, to summarize existing studies assessing chemical exposure in human fetal organs, and to discuss possible interactions between physiological changes and exposures. Our review reveals major knowledge gaps in factors affecting fetal chemical exposure, highlighting the need to develop more sophisticated tools for chemical health risk assessment in fetuses.

The effects of progesterone on immune cellular function at the maternal-fetal interface and in maternal circulation

Progesterone is a sex steroid hormone that plays a critical role in the establishment and maintenance of pregnancy. This hormone drives numerous maternal physiological adaptations to ensure the continuation of pregnancy and to facilitate fetal growth, including broad and potent modulation of the maternal immune system to promote maternal-fetal tolerance. In this brief review, we provide an overview of the immunomodulatory functions of progesterone in the decidua, placenta, myometrium, and maternal circulation during pregnancy. Specifically, we summarize current evidence of the regulated functions of innate and adaptive immune cells induced by progesterone and its downstream effector molecules in these compartments, including observations in human pregnancy and in animal models. Our review highlights the gaps in knowledge of interactions between progesterone and maternal cellular immunity that may direct future research.

Maternal physiologic adaptations during transport

Maternal physiologic adaptations during maternal transportation are not well understood. We sought to describe the fetal and maternal changes during maternal transport as described by maternal physiologic parameters, according to transport type.

Here and there a trophoblast, a transcriptional evaluation of trophoblast cell models.

A recent explosion of methods to produce human trophoblast and stem cells (hTSCs) is fuelling a renewed interest in this tissue. The trophoblast is critical to reproduction by facilitating implantation, maternal physiological adaptations to pregnancy and the growth of the fetus through transport of nutrients between the mother and fetus. More broadly, the trophoblast has phenotypic properties that make it of interest to other fields. Its angiogenic and invasive properties are similar to tumours and could identify novel drug targets, and its ability to regulate immunological tolerance of the allogenic fetus could lead to improvements in transplantations. Within this review, we integrate and assess transcriptomic data of cell-based models of hTSC alongside in vivo samples to identify the utility and applicability of these models. We also integrate single-cell RNA sequencing data sets of human blastoids, stem cells and embryos to identify how these models may recapitulate early trophoblast development.

Nutrient Requirements during Pregnancy and Lactation.

A woman’s nutritional status during pregnancy and breastfeeding is not only critical for her health, but also for that of future generations. Nutritional requirements during pregnancy differ considerably from those of non-pregnant women. Thus, a personalized approach to nutritional advice is recommended. Currently, some countries recommend routine supplementation for all pregnant women, while others recommend supplements only when necessary. Maternal physiological adaptations, as well as nutritional requirements during pregnancy and lactation, will be reviewed in the literature examining the impacts of dietary changes. All of these data have been studied deeply to facilitate a discussion on dietary supplement use and the recommended doses of nutrients during pregnancy and lactation. The aim of this review is to evaluate the knowledge in the scientific literature on the current recommendations for the intake of the most common micronutrients and omega-3 fatty acids during pregnancy and lactation in the United States, Canada, and Europe. Taking into account these considerations, we examine minerals, vitamins, and omega-3 fatty acid requirements. Finally, we conclude by discussing the potential benefits of each form of supplementation.

Regulation of maternal-fetal metabolic communication.

Pregnancy may be the most nutritionally sensitive stage in the life cycle, and improved metabolic health during gestation and early postnatal life can reduce the risk of chronic disease in adulthood. Successful pregnancy requires coordinated metabolic, hormonal, and immunological communication. In this review, maternal-fetal metabolic communication is defined as the bidirectional communication of nutritional status and metabolic demand by various modes including circulating metabolites, endocrine molecules, and other secreted factors. Emphasis is placed on metabolites as a means of maternal-fetal communication by synthesizing findings from studies in humans, non-human primates, domestic animals, rabbits, and rodents. In this review, fetal, placental, and maternal metabolic adaptations are discussed in turn. (1) Fetal macronutrient needs are summarized in terms of the physiological adaptations in place to ensure their proper allocation. (2) Placental metabolite transport and maternal physiological adaptations during gestation, including changes in energy budget, are also discussed. (3) Maternal nutrient limitation and metabolic disorders of pregnancy serve as case studies of the dynamic nature of maternal-fetal metabolic communication. The review concludes with a summary of recent research efforts to identify metabolites, endocrine molecules, and other secreted factors that mediate this communication, with particular emphasis on serum/plasma metabolomics in humans, non-human primates, and rodents. A better understanding of maternal-fetal metabolic communication in health and disease may reveal novel biomarkers and therapeutic targets for metabolic disorders of pregnancy.

Effectiveness of tendoachilles and hamstring stretching on nocturnal leg cramps among antenatal women

Pregnancy also known as gravidity, is the duration which one or more offspring develops inside a woman. A multiple pregnancy involves more than one offspring, such as with twins. Pregnancy can occur by sexual intercourse or assisted reproductive technology. In the pregnancy which lasts about 40 weeks, is grouped into three trimesters. Maternal physiologic adaptations are attributed to the hormones of pregnancy and to mechanical pressures arising from the enlarging uterus and other tissues. These adaptations protect the woman’s normal physiologic functioning, meet the metabolic demands pregnancy imposes on her body, and provide a nurturing environment for foetal development and growth. Although pregnancy is a normal phenomenon, problems can occur. The hormonal and physical changes of pregnancy result in enormous changes in a woman’s body. Enormous amount of estrogen is produced which leads to the discomforts during pregnancy. Common musculoskeletal discomforts are back pain, sacroiliac joint dysfunction, leg cramps, nerve compression syndromes like carpel tunnel syndrome, brachial plexus pain, meralgia paraesthetica, posterior tibial nerve compression, circulatory disorder such as varicose vein in the legs, vulval varicose vein, haemorrhoids, cramp, thrombosis and thrombo embolism, thoracic outlet syndrome, thoracic spine pain, postural back ache, osteoporosis of pregnancy, fatigue, insomnia and nightmares.

The Role of Placental Hormones in Mediating Maternal Adaptations to Support Pregnancy and Lactation

During pregnancy, the mother must adapt her body systems to support nutrient and oxygen supply for growth of the baby in utero and during the subsequent lactation. These include changes in the cardiovascular, pulmonary, immune and metabolic systems of the mother. Failure to appropriately adjust maternal physiology to the pregnant state may result in pregnancy complications, including gestational diabetes and abnormal birth weight, which can further lead to a range of medically significant complications for the mother and baby. The placenta, which forms the functional interface separating the maternal and fetal circulations, is important for mediating adaptations in maternal physiology. It secretes a plethora of hormones into the maternal circulation which modulate her physiology and transfers the oxygen and nutrients available to the fetus for growth. Among these placental hormones, the prolactin-growth hormone family, steroids and neuropeptides play critical roles in driving maternal physiological adaptations during pregnancy. This review examines the changes that occur in maternal physiology in response to pregnancy and the significance of placental hormone production in mediating such changes.

The Association of Maternal Exposure to Domestic Violence During Childhood With Prenatal Attachment, Maternal-Fetal Heart Rate, and Infant Behavioral Regulation.

Human and animal models suggest that maternal hormonal and physiological adaptations during pregnancy shape maternal brain functioning and behavior crucial for offspring care and survival. Less sensitive maternal behavior, often associated with psychobiological dysregulation and the offspring's behavioral and emotional disorders, has been observed in mothers who have experienced adverse childhood experiences. Strong evidence shows that children who are exposed to domestic violence (DV) are at risk of being abused or becoming abusive in adulthood. Yet little is known about the effect of childhood exposure to DV on the expecting mother, her subsequent caregiving behavior and related effects on her infant. Thus, the present study examined the association of maternal exposure to DV during childhood on prenatal maternal attachment, maternal heart rate reactivity to an infant-crying stimulus and post-natal infant emotional regulation. Thirty-three women with and without exposure to DV during childhood were recruited during the first trimester of pregnancy and followed until 6-month after birth. The Maternal Antenatal Attachment Scale (MAAS) was used to measure prenatal attachment of the mother to her fetus during the second trimester of pregnancy, maternal and fetal heart rate reactivity to an infant-crying stimulus was assessed at the third trimester of pregnancy, and the Infant Behavior Questionnaire-Revised (IBQ-R) was used to assess infant emotional regulation at 6-months. Results showed that pregnant women that were exposed to DV during childhood had a poorer quality of prenatal attachment of mother to fetus, regardless of whether they also experienced DV during adulthood. In addition, maternal exposure to DV during childhood was associated with increased maternal heart rate to infant-crying stimulus and worse infant emotional regulation. These findings highlight the importance of prenatal screening for maternal exposure to DV during childhood as a risk factor for disturbances in the development of maternal attachment, dysfunctional maternal behavior and emotion dysregulation.

The murine female intestinal microbiota does not shift throughout the estrous cycle.

Pregnancy is accompanied by maternal physiological adaptations including metabolic, endocrine, immune, cardiovascular, skeletomuscular and neurological modifications that facilitate fetal and placental growth and development. Emerging evidence suggests that the maternal intestinal microbiota is modified over the course of healthy pregnancy. We have recently identified a maternal intestinal microbial shift within hours of conception; a shift that continued with advancing gestation. It is possible that maternal gut bacterial profiles might be associated with the known endocrine changes that accompany the female reproductive (estrous) cycle. Methods: To determine whether the estrous cycle influenced the shifts in the maternal intestinal microbiota, time-matched fecal pellets were collected daily for 3 consecutive estrous cycles from individually housed, non-pregnant female C57BL/6J mice (n = 10) fed a control diet. Estrous stage was identified by cell type predominance in vaginal cytological samples. The corresponding fecal pellets for each estrous stage were processed for bacterial 16S rRNA sequencing of the variable 3 (V3) region. Results: Estrous cycle stage accounted for a very small and not statistically significant proportion of the variation in the fecal microbiota according to PERMANOVA testing performed on Bray-Curtis dissimilarity scores. These values displayed no significant clustering of fecal microbial communities by estrous stage. Conclusion: The estrous cycle does not result in any significant shift in the intestinal microbial community in the reproductively mature, regularly cycling female mouse.

Identifying Maternal Constraints on Fetal Growth and Subsequent Perinatal Outcomes Using a Multiple Embryo Implantation Model.

IntroductionAlthough the majority of singleton births after in vitro fertilization (IVF) are uncomplicated, studies have suggested that IVF pregnancies may be independently associated with low birth weight (LBW), preterm birth (PTB), and perinatal mortality. These outcomes complicate multiple gestations as expected, but have also been reported in singletons. A multiple embryo implantation model allows for assessment of the early in utero environment, and therefore, assessment of any maternal constraints on developing fetuses. We question whether adverse perinatal outcomes associated with assisted reproductive techniques (ART) occur as a result of maternal physiologic adaptations.Patients and MethodsThis is a retrospective, single center study of ART cycles, specifically intracytoplasmic sperm injection (ICSI) cycles during a 16-year period. For each positive pregnancy test 9–11 days after embryo transfer, an ultrasonogram was performed at 7 weeks of gestation to record the number of implanted fetal poles with cardiac activity. Controlled ovarian stimulation (COS), hCG trigger, oocyte retrieval and sperm injection were performed as per our standard protocols. First trimester implantation sites that resulted in live births were defined as “true” to distinguish them from those that spontaneously reduced called “virtual.” Birth outcomes analyzed included birth weight and gestational age at delivery.ResultsA total of 17,415 cycles were analyzed. The average maternal age was 36.9 (±5.0) years. An overall fertilization rate of 73.4% generated approximately 48,708 good quality cleavage-stage embryos. In most patients (92.8%), an average of 3 embryos were transferred. The clinical pregnancy rate was 39.2% (n = 6,281). The overall occurrence of multiple gestations was 38.2% (n = 2,608) consisting of 2,038 twin, 511 triplet, and 59 quadruplet pregnancies. Of these multiple gestations, 18.6% of twin, 54.2% of triplet and 76.3% of quadruplet gestations spontaneously reduced. Failure of the implanted embryo to progress was not related to maternal age. Singleton newborns resulting from multiple implantation sites had lower birth weights (P<0.01) and shorter gestational ages (P<0.01) than those from a single implanted embryo. The number of embryos transferred did not affect the gestational length of singleton newborns. Although the birth weights of singletons from multiple implantation sites (virtual singletons) were lower than true singletons, the birth weight of virtual singletons were comparable to the birth weights of true twin, triplet, and quadruplet live births. Multiple logistic regression revealed that virtual singletons were an independent risk factor for PTB (odds ratio: 4.55, 95% CI 2.23–9.29) and LBW (odds ratio: 3.61, 95% CI 1.78–7.32), even after controlling for the number of oocytes, stimulation protocol type, sperm source, total gonadotropins administered, age, embryo quality, and day of embryo transfer.ConclusionsOur study highlights that embryonic implantation sites during early gestation set the growth profile of each embryo, dictating later growth patterns. Specifically, spontaneous reduction of an embryo after multiple embryo implantations can confer greater perinatal risk in the form of LBW and PTB to the surviving fetus. Our findings suggest that maternal constraints or physiologic adaptations maybe one of the mechanisms mediating adverse perinatal outcomes when multiple embryo implantation occurs.

Trophoblastic debris modifies endothelial cell transcriptome in vitro: a mechanism by which fetal cells might control maternal responses to pregnancy.

The mechanisms by which the fetus induces maternal physiological adaptations to pregnancy are unclear. Cellular debris, shed from the placental syncytiotrophoblast into the maternal blood and phagocytosed by maternal endothelial and immune cells, may be one of these mechanisms. Here we show that trophoblastic debris from normal first trimester placentae induces changes in the transcriptome and proteome of endothelial cells in vitro, which might contribute to the adaptation of the maternal cardiovascular system to pregnancy. Trophoblastic debris also induced endothelial cells to transcribe placenta-specific genes, including the vasodilator hormone CSH1, thereby expanding the effective functional size of the placenta. Our data suggest that the deportation of trophoblastic debris is an important part of the complex network of feto-maternal communication.

G-Protein-coupled receptors as potential drug candidates in preeclampsia: targeting the relaxin/insulin-like family peptide receptor 1 for treatment and prevention.

Important roles for G-protein-coupled receptors (GPCRs) have been identified in the maternal physiological adaptations to pregnancy and in the pathogenesis of preeclampsia. On this basis, GPCRs are potential therapeutic targets for preeclampsia. In this review, vasopressin and apelin are initially considered in this context before the focus on the hormone relaxin and its cognate receptor, the relaxin/insulin-like family peptide receptor 1 (RXFP1). Based on both compelling scientific rationale and a promising safety profile, the relaxinligand-receptor system is comprehensively evaluated as a potential therapeutic endpoint in preeclampsia. The published literature relating to the topic was searchedthroughJanuary 2016 using PubMed. Relaxin is a peptide hormone secreted by the corpus luteum; it circulates in the luteal phase and during pregnancy. Activation of RXFP1 is vasodilatory; thus, relaxin supplementation is expected to at least partly restore the fundamental vasodilatory changes of normal pregnancy, thereby alleviating maternal organ hypoperfusion, which is a major pathogenic manifestation of severe preeclampsia. Specifically, by exploiting its pleiotropic hemodynamic attributes in preeclampsia, relaxin administration is predicted to (i) reverse robust arterial myogenic constriction; (ii) blunt systemic and renal vasoconstriction in response to activation of theangiotensin II receptor, type 1; (iii) mollify the action of endogenous vasoconstrictors on uterine spiral arteries with failed remodeling and retained smooth muscle; (iv) increase arterial compliance; (v) enhance insulin-mediated glucose disposal by promoting skeletal muscle vasodilation and (vi) mobilize and activate bone marrow-derived angiogenic progenitor cells, thereby repairing injured endothelium and improving maternal vascularity in organs such as breast, uterus, pancreas, skin and fat. By exploiting its pleiotropic molecular attributes in preeclampsia, relaxin supplementation is expected to (i) enhance endothelial nitric oxide synthesis and bioactivity, as well as directly reduce vascular smooth muscle cytosolic calcium, thus promoting vasodilation; (ii) improve the local angiogenic balance by augmenting arterial vascular endothelial and placental growth factor (VEGF and PLGF) activities; (iii) ameliorate vascular inflammation; (iv) enhance placental peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PCG1α) expression, and hence, peroxisome proliferator-activated receptor gamma(PPAR-γ) activity and (v) confer cytotrophoblast and endothelial cytoprotection. Insofar as impaired endometrial maturation (decidualization) predisposes to the development of preeclampsia, relaxin administration in the late secretory phase and during early pregnancy would be anticipated to improve decidualization, and hence trophoblast invasion and spiral artery remodeling, thereby reducing the risk of preeclampsia. Relaxin has a favorable safety profile both in the non-pregnant condition and during pregnancy. There is a strong scientific rationale for RXFP1 activation in severe preeclampsia by administration of relaxin, relaxin analogs or small molecule mimetics, in order to mollify the disease pathogenesis for safe prolongation of pregnancy, thus allowing time for more complete fetal maturation, which is a primary therapeutic endpoint in treating the disease. In light of recent data implicating deficient or defective decidualization as a potential etiological factor in preeclampsia and the capacity of relaxin to promote endometrial maturation, the prophylactic application of relaxin to reduce the risk of preeclampsia is a plausible therapeutic approach to consider. Finally, given its pleiotropic and beneficial attributes particularly in the cardiovascular system, relaxin, although traditionally considered as a 'pregnancy' hormone, is likely to prove salutary for several disease indications in the non-pregnant population.

Pregnancy-induced adaptations of the central circadian clock and maternal glucocorticoids.

Maternal physiological adaptations, such as changes to the hypothalamic-pituitary-adrenal (HPA) axis, are central to pregnancy success. Circadian variation of the HPA axis is dependent on clock gene rhythms in the hypothalamus, but it is not known whether pregnancy-induced changes in maternal glucocorticoid levels are mediated via this central clock. We hypothesized that hypothalamic expression of clock genes changes across mouse pregnancy and this is linked to altered HPA activity. The anterior hypothalamus and maternal plasma were collected from C57Bl/6J mice prior to pregnancy and on days 6, 10, 14 and 18 of gestation (term=d19), across a 24-h period (0800, 1200, 1600, 2000, 0000, 0400 h). Hypothalamic expression of clock genes and Crh was determined by qPCR, plasma ACTH concentration measured by Milliplex assay and plasma corticosterone concentration by LC-MS/MS. Expression of all clock genes varied markedly across gestation, most notably at mid-gestation when levels of each gene were elevated. The pregnancy-induced increase in maternal corticosterone levels (by up to 14-fold on day 14) was not accompanied by a parallel shift in plasma ACTH (28% lower on day 14 compared with non-pregnant levels). Moreover, while circadian rhythmicity in corticosterone was maintained up to day 14 of gestation, this was effectively lost by day 18. Overall, our data show that the central circadian clock undergoes marked adaptations throughout mouse pregnancy, changes that are likely to contribute to maternal physiological adaptations. Importantly, however, neither hypothalamic clock genes nor plasma ACTH levels appear to drive the marked increase in maternal corticosterone after mid-gestation.

Circadian Variation in Placental and Hepatic Clock Genes in Rat Pregnancy

Clock genes drive circadian rhythms in a range of physiological processes both centrally and in peripheral tissues such as the liver. The aims of this study were to determine whether the two functionally-distinct zones of the rat placenta (junctional and labyrinth) differentially express clock genes and, if so, whether these exhibit circadian patterns. Rats were sampled from d 21 of pregnancy (term = d 23) and from diestrus I of the estrous cycle. Adult liver (all animals), fetal liver, and placental zones (pregnant animals) were collected at 0800, 1400, 2000, and 0200 h. Both zones of the rat placenta expressed all seven canonical clock genes (Clock, Bmal1, Per1, Per2, Per3, Cry1, and Cry2), but there were marked zonal differences and, unlike in maternal liver, circadian variation in placenta was limited. Similarly, placental expression of Vegf varied with zone but not time of day. Pregnancy also led to marked changes in hepatic clock gene expression, with peak levels of Per1, Cry1, and Cry2 all reduced, Per3 increased, and circadian variation in Clock expression lost. All clock genes were expressed in fetal liver, but there was less circadian variation than in maternal liver. Similarly, fetal corticosterone levels remained stable across the day, whereas maternal corticosterone showed clear circadian variation. In conclusion, our data show that the rat placenta expresses all canonical clock genes in a highly zone-specific manner but with relatively little circadian variation. Moreover, pregnancy alters the expression and circadian variation of clock genes in maternal liver, possibly contributing to maternal physiological adaptations.

Pode a atividade física materna modular a programação fetal induzida pela nutrição?

Existe considerável evidência para a indução de diferentes fenótipos em reposta às variações no ambiente fetal e neonatal. O aporte inadequado de nutrientes no período crítico do desenvolvimento está associado ao risco alto de doenças metabólicas na vida adulta, este fenômeno biológico é chamado de programação. A atividade física durante a gestação resulta em adaptações fisiológicas da mãe e no aumento da disponibilidade de nutrientes e oxigênio no espaço feto-placentário. Este trabalho tem como objetivo discutir os mecanismos da indução de programação fetal pela nutrição e o provável efeito modulador da atividade física durante a gestação. Foram utilizadas as bases de dados do Medline Pubmed, Lilacs e Bireme, com publicações entre 1990 até 2008. Os termos de indexação utilizados foram: nutrition, fetal programming, gestation, physical activity, physical exercise, metabolism. Em conclusão, o aporte inadequado de nutrientes programa o aparecimento de doenças metabólicas na vida adulta, enquanto que a atividade física durante a gestação aumenta a disponibilidade de nutrientes e oxigênio, repercutindo positivamente no crescimento fetal e no peso ao nascer.

Physiological adaptation in early human pregnancy: adaptation to balance maternal-fetal demands

After conception, the corpus luteum, placenta, and developing embryo release hormones, growth factors, and other substances into the maternal circulation. These substances trigger a cascade of events that transform the functioning of the maternal cardiovascular, respiratory, and renal systems, which in turn alter the physicochemical determinants of [H(+)]. Following implantation, maternal adaptations fulfill 4 important functions that support fetal growth. Increased availability of substrates and precursors for fetal-placental metabolism and hormone production is mediated by increases in dietary intake, as well as endocrine changes that increase the availability of glucose and low-density lipoprotein (LDL) cholesterol. Transport capacity is enhanced by increases in cardiac output, facilitating the transport of substrates and precursors to the placenta, and fetal waste products to maternal organs for disposal. Maternal-fetal exchange is regulated by the placenta after 10-12 weeks gestation, but it may occur through histiotrophic mechanisms before this time. Disposal of additional waste products (heat, carbon dioxide, and metabolic byproducts) occurs through peripheral vasodilation and increases in skin blood flow, ventilation, and renal filtration. The maternal physiological adaptations described above must meet the combined demands of maternal exercise and fetal growth. More research is needed to formulate evidence-based guidelines for healthy physical activity in early pregnancy.

Establishing the Criteria for Anesthesia and Other Precautions for Surgery During Pregnancy

Surgical procedures may be undertaken in the gravida with relatively little risk to the fetus or the continuation of pregnancy. The managing physician requires a thorough knowledge of the maternal physiologic adaptations to pregnancy to minimize maternal iatrogenic risks. The potential fetal effects of the planned procedure, diagnostic tests, therapeutic drugs, and anesthesia must be considered preoperative. Any potential fetal risks must be discussed with the patient and, in some cases, maternal need may obviate undertaking some procedures that place the fetus at some jeopardy. The outcome in most situations of surgery on the gravida is good for both the mother and the fetus.

The changing thermal response to endurance exercise during pregnancy

This study was designed to test the hypothesis that the thermal response to endurance exercise is altered by the thermal adaptations to pregnancy. Accordingly, rectal temperature was monitored in 18 recreational athletes before, during, and after 20 minutes of continuous exercise before conception and every 6 to 8 weeks during pregnancy. Mean exercise intensity was 64% of Vo2 max before conception and did not change during pregnancy. However, the peak rectal temperature reached during exercise decreased by 0.3° C at 8 weeks and then fell at a rate of 0.1° C per lunar month through the thirty-seventh week. This appeared to be related to changes in resting temperature, thermal mass, sweating threshold, and venous capacitance that began early in pregnancy. These data suggest that the magnitude of any exercise-associated thermal stress for the embryo and fetus is markedly reduced by the maternal physiologic adaptations to pregnancy. (AM J OBSTET GYNECOL 1991;165:1684-9.)

6 Diabetes and diet in pregnancy

The mean additional energy requirement for pregnancy has been calculated at 285 kcal daily and it reflects the energy needs for production of the fetoplacental unit and for the maternal physiological adaptations to pregnancy. In practice there is considerable variation in energy requirement due to alterations in maternal energy expenditure. Optimal energy intakes are dictated also by the pre-pregnancy maternal weight. The outcome of pregnancy is improved in the underweight mother by an intake which produces a weight gain in pregnancy of approximately 14 kg, whereas a rise of only 7 kg may be optimal for the obese mother. Obesity with or without diabetes is associated with macrosomia and other problems and it is sensible to attempt to limit weight gain in pregnancy at a time when maternal motivation is high. Diabetes in pregnancy may arise in patients with pre-existing NIDDM or IDDM, but more commonly it is diagnosed for the first time during pregnancy and it usually disappears after delivery (gestational diabetes). Recent evidence suggests that gestational diabetes has a strong genetic component and is usually NIDDM precipitated early in life by the pregnancy. Both gestational diabetes and NIDDM are characterized by insulin deficiency and by insulin resistance. Long-term follow-up studies have demonstrated that NIDDM or impaired glucose tolerance develop in later life in 50-70% of women with previous gestational diabetes. The adverse effects of pregnancy on the mother with pre-existing diabetes may be minimized by good diabetic control as may be adverse effects on the fetus and neonate of diabetes in the mother. An increased incidence of fetal malformations persists in pregnancies with pre-existing maternal diabetes. Diabetes of any form may be associated with neonatal hypoglycaemia. The aim of therapy is to produce maternal normoglycaemia throughout pregnancy by dietary measures and insulin treatment if required. Women with pre-existing diabetes should tighten their blood glucose control from before conception. Optimization of insulin therapy and diet are required for IDDM and most NIDDM women will require insulin treatment in pregnancy. Gestational diabetics require diet and possibly insulin. Most pregnancies now proceed to term.